Retinoic acid (RA) and fibroblast growth factor 10 (Fgf10) are known to be important for lung development. Recent data from our lab show that one of the roles of RA is to induce Fgf10 expression in the primitive foregut to trigger primary lung bud formation. How RA influences Fgf10 expression is unclear. To start addressing this issue, I performed a genome-wide oligonucleotide microarray analysis of RA targets in the developing foregut using two models of RA-deficiency. Unexpectedly, a statistically-significant number of components and targets of transforming growth factor-beta (Tgfb) signaling were found to be upregulated when RA signaling is disrupted. Given the microarray data and the previous reports suggesting that Tgfbl is a negative regulator of Fgfl0, I hypothesize that, during normal development, RA serves to tightly control Tgfbl signaling, thereby allowing Fgf10 expression to occur in the prospective lung field of the foregut, and trigger primary lung bud formation. I will address this hypothesis by 1) characterize mechanisms by which RA-Tgfb1, and Tgfb1-Fgf10 interact during primary lung budding; and 2) investigate the functional link between RA-Tgfb1 -Fgf10 and lung bud initiation.